Chlamydia trachomatis is the leading cause of bacterial sexually transmitted disease worldwide resulting in 4-5 million new cases of Chlamydia annually and an estimated 100 million cases per annum. Infections of the lower female genital tract (FGT) frequently are asymptomatic; thus, they often remain undiagnosed or untreated. If infections are either not resolved or left untreated, chlamydia can ascend to the upper FGT and infect the fallopian tubes (FTs) causing salpingitis that may lead to functional damage of the FTs and tubal factor infertility (TFI). Clinical observations and experimental data have indicated a role for antibodies against C. trachomatis proteins such as the 60-kDa heat shock protein 60 (cHSP60) in the immunopathogenesis of TFI. When released from infected cells, cHSP60 can induce proinflammatory immune responses that may functionally impair the FTs leading to fibrosis and luminal occlusion. Chlamydial pathogenesis of irreversible and permanent tubal damage is a consequence of innate and adaptive host immune responses to ongoing or repeated infections. The extracellular matrix that is regulated by metalloproteinases may also be modified by chlamydial infections of the FGT. This review will highlight protective and pathogenic immune responses to ongoing and repeated chlamydial infections of the FGT. It will also present two recent hypotheses to explain mechanisms that may contribute to FT damage during a C. trachomatis infection. If Chlamydia immunopathology can be controlled, it might yield a method of inducing fibrosis and thus provide a means of nonsurgical permanent contraception for women.
Keywords: Chlamydia trachomatis; Fallopian tube damage; Fibrosis; Immunopathogenesis.
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